The objective of the proposed work is to more clearly define the cellular mechanisms involved in the development and regression of neonatal cardiac enlargement and to determine if these mechanisms influence the functional state of the heart. Pressure overload cardiac enlargement will be created in 14-day old rats by constricting the abdominal aorta. Cellular proliferation during cardiac enlargement will be evaluated by determining left ventricular DNA content. Proliferating cardiac muscle cells and/or interstitial cells will be identified by connective tissue measurements and radioautography. Functional measurements will be taken in enlarged hearts using an in situ rat heart preparation. Aortic constriction will also be surgically removed at the point of "stable" cardiac enlargement to obtain similar information during the regression process. In addition, moderate exercise will be imposed during regression of cardiac enlargement to determine whether the rate of regression, the cellular composition of the regressed heart and its function-contractile state can be influenced. BIBLIOGRAPHIC REFERENCES: Dowell, R. T., A. F. Cutilletta, M. A. Rudnik and P. C. Sodt: Heart functional responses to pressure overload in exercised and sedentary rats. Am. J. Physiol. 230: 199-204, 1976. Dowell, R. T.: Depressed myocardial contractility and myofibrillar ATPase activitY in chemically sympathectomized rats. Fed. Proc. 35:613, 1976. (Abstract)